March 22 - Cardiology Flashcards
Endothelium-mediated vasodilation
- ACh, bradykinin, serotonin, substance P, shear forces increase Ca++ leading to eNOS activation
- eNOS synthesizes NO from argininine, NADPH, and O2
- NO activates guanalyl cyclase, increasing cGMP and decreasing Ca++ in VSMC and decreasing contraction
ARB MOA
blocks ang II receptors. Ang II levels increase but its effects are blocked
Aortic regurn
Early diastolic murmur. Duration of murmur indicative of severity. Most common cause is aortic root dilation
Small vs large VSD
Small
- holosystolic murmur at L sternal border
- insignificant, close spontaneously
Large
- no murmur
- failure to thrive, diaphoresis with feeding
Why CCBs don’t affect skeletal muscle
Skeletal muscle not dependent on extracellular Ca++. It is the interaction between L-type Ca++ channels in the plasma membrane and RyR channels in the SR that matters
Pathologic progression post-MI
First 4 hours: normal myocardium
4-12 hours: cytoplasmic hypereosinophilia, edema, punctate hemorrhage (early coag necrosis)
12-24 hours: continued coag necrosis, marginal contraction band necrosis
1-5 days: coag necrosis + neutrophil infiltrate
5-10 days: macrophages
10-14 days: granulation tissue and neovascularization
2 wks to 2 mos: scar formation
Doxorubicin cardiotoxicity
Causes dilated cardiomyopathy. Prevented with dexrazoxane (iron chelator that decreases free radical formation)
Nitrate dosing
Round the clock nitrates results in rapid development of tolerance. Thus, when nitrates used chronically, provide a daily nitrate-free interval typically overnight
Use dependence of different class I antiarrythmics
Highest with class IC due to slow dissociation/strongest binding strength to Na+ channels. IB dissociate the most rapidly due to weakest binding strength
Causes of S3 heart sound
- Forceful or rapid filling
- Decreased ventricular compliance
3) Increased ESV
Pulmonary HTN due to LHF: pathogenesis
Pulmonary venous congestion increases pulmonary capillary and arterial pressure. High pressures damage the endothelium, increasing vascular tone and causing remodeling with smooth muscle proliferation
Janeway lesions
Nontender macules on the palms and soles caused by septic emboli from valvular vegetations
Signs of acute vs chronic pericarditis
Acute: pleuritic chest pain, pericardial friction rub
Chronic (months to years): paradoxic increase in JVP with inspiration, pulsus paradoxus, pericardial knock
pulsus paradoxus
Decrease in systolic BP greater thn 10 during inspiration. Associated with cor pulmonale, chronic constrictive pericarditis, cardiac tamponade
Atherosclerosis pathogenesis
- Endothelial cell injury. Can be caused by HTN, hyperlipidemia, smoking, diabetes, others
- Increased vascular permeability allows for leukocyte adhesion and migration. Exposure of subendothelial collagen allows for platelet adhesion.
- Medial smooth muscle migrates to the intima. LDL also migrates to intima and is endocytosed by macrophages yielding foam cells.
- Chronic inflammatory state is maintained by macrophage and lymphocyte release of cytokines and growth factors. These cause continued deposition of LDL, SMC proliferation and production of more ECM, and foam cell necrosis and release of lipids into the intima ECM
Varicose veins: pathogenesis, risk factors, complications
Pathogenesis: Increased pressure results in venous dilation causing stretching and failure of the venous valves. Results in venous stasis, congestion, and lower extremity edema.
Risk factors: Long periods of standing, age over 50, obesity, multiple pregnancies (all things that increase venous pressure in legs chronically)
Complications: Thromboses, stasis dermatitis, skin ulcers, poor wound healing, superficial infection. No risk of DVT or PE because varicosities are in superficial, not deep veins
Pericardial disease: etiology
Infection
Autoimmune - RA, SLE, Dressler syndrome post-MI
Direct trauma
Cancer - lung, breast, esophageal, lymphoma
Acute pericarditits
Inflammatin of pericardium. Presents with friction rub and pleuritic, positional chest pain. Detected on EKG with global ST elevation and PR depression. Treated wtih anti-inflammatories (NSAIDs first, glucocorticoids if ineffective)
Pericardial effusion
Fluid between pericardium and myocardium. Ranges from mild to cardiac tamponade at severe end. Can be due to underlying pericarditis or to traumatic injury or ventricular free wall rupture after MI. Hemodynamic problem: pressure prevents ventricular filling. Treatment is fliuds which can help with ventricular filling, treating underlying etiology, and/or pericardiocentesis/surgery
Chronic pericarditis
Result of chronic pericardial inflammation that leads to fibrosis of pericardium. Can prevent diastolic filling. Pericardial knock results from relaxation of ventricle against fibrotic pericardium. Anatomic problem with anatomic solution (removal of pericardium)
MOA of ANP and BNP
Activate guanylate cyclase, increasing cGMP, leading to vasodilation. Also cause diuresis.
Myocardial hybernation
State of chronic myocardial ischmiea Myocardial metabolism and function decrease to match the decrease seen in coronary bood flow. Prevents myocardial necrosis
Isolated atrial amyloidosis
Deposition of abnormally folded ANP. Incidence increases with age. Can increase risk of afib
Statin MOA
Inhibits hepatic cholesterol synthesis. LDL receptor expression increases in liver leading to increased LDL uptake and lower serum cholesterol and LDL
Osler-Weber-Rendu syndrome
another name for HHT
Von recklinghausen’s disease
another name for NF1
EKG patterns for different MIs
PDA occlusion: causes inferior wall ischemia which manifests as ST elevation in II, III, and aVF
LAD occliusion: causes anterior wall ischemia which manifests as ST elevation in V1-V4
LCX occlusion: causes lateral wall ischemia which manifests as ST elevation in V5-V6, sometimes I and aVL
LPL
Enzyme that hydrolyzes TGs, releasing FFAs and facilitates cholesterol transfer to HDL
Cardiac myxoma
Most commonly arises in LA as a large, gelatinous, pedunculated mass. Histology shows scattered cells in mucopolysaccharide stroma, abnormal BVs, and hemorrhage. Presents with constitutional symptoms, murmur, and positional dyspnea due to valve obstruction
Kussmaul sign
Volume constricted RV in chronic pericarditis can’t accomodate increased venous return during inspiration, resulting in JVD
